Zika virus and GLUT1

Blonz, Edward R.

doi:10.1016/s1473-3099(16)30062-7

Cited by 10 publications

(8 citation statements)

References 7 publications

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“…For example, the Zika virus, associated with human congenital fetal anomalies, diverts host cell resources and reprograms metabolic processes to support RNA metabolism, ATP production, and glycolysis. This metabolic state is conducive for Zika virus replication 67 and may control access to nutrients (for example, glucose), a requisite for endothelial growth within the placenta and fetal development 68 . Non-viral pathogens such as Plasmodium berghei , a malarial parasite of rodents, augment glucose uptake via Glut1 activity and surface localization in infected hepatic cells as an adaptive response for survival 69 .…”

Section: Intracellular Pathogens Have a Sweet Tooth For Survivalmentioning

confidence: 99%

Exploiting immune cell metabolic machinery for functional HIV cure and the prevention of inflammaging

et al. 2018

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An emerging paradigm in immunology suggests that metabolic reprogramming and immune cell activation and functions are intricately linked. Viral infections, such as HIV infection, as well as cancer force immune cells to undergo major metabolic challenges. Cells must divert energy resources in order to mount an effective immune response. However, the fact that immune cells adopt specific metabolic programs to provide host defense against intracellular pathogens and how this metabolic shift impacts immune cell functions and the natural course of diseases have only recently been appreciated. A clearer insight into how these processes are inter-related will affect our understanding of several fundamental aspects of HIV persistence. Even in patients with long-term use of anti-retroviral therapies, HIV infection persists and continues to cause chronic immune activation and inflammation, ongoing and cumulative damage to multiple organs systems, and a reduction in life expectancy. HIV-associated fundamental changes to the metabolic machinery of the immune system can promote a state of “inflammaging”, a chronic, low-grade inflammation with specific immune changes that characterize aging, and can also contribute to the persistence of HIV in its reservoirs. In this commentary, we will bring into focus evolving concepts on how HIV modulates the metabolic machinery of immune cells in order to persist in reservoirs and how metabolic reprogramming facilitates a chronic state of inflammation that underlies the development of age-related comorbidities. We will discuss how immunometabolism is facilitating the changing paradigms in HIV cure research and outline the novel therapeutic opportunities for preventing inflammaging and premature development of age-related conditions in HIV + individuals.

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Section: Intracellular Pathogens Have a Sweet Tooth For Survivalmentioning

confidence: 99%

Exploiting immune cell metabolic machinery for functional HIV cure and the prevention of inflammaging

et al. 2018

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“…Glut1 upregulation may be linked to other pathological events independent of its functional role on immune cells. Recently, Blonz 23 theorized that Zika virus causes microcephaly by disturbing the placental Glut1 expression which limits access to glucose needed for normal fetal growth. This view is supported by observations that a genetic Glut1 deficiency is associated with an increased risk of acquired microcephaly in infants.…”

Section: Immunometabolic Regulations In Other Virusesmentioning

confidence: 99%

Metabolic reprogramming during hepatitis B disease progression offers novel diagnostic and therapeutic opportunities

Masson

Billings

Palmer

2017

Antivir Chem Chemother

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Metabolic remodeling occurs in immune cells during an infection. Host cells must upregulate energy production for growth, proliferation, and effector functions to limit the damage imposed by pathogens. One example, the hepatitis B virus, induces hepatic injury in human hepatocytes through dysregulation of aerobic glycolysis and lipid metabolism. Increased glycolytic metabolism mediated by elevated expression of Glut1, glucose influx, and lactate secretion is associated with this Warburg phenotype, a classic metabolic signature also observed in cancer cells. This article brings into focus the tight interaction between HBV infection and metabolic dysfunction and how these processes facilitate the progression of end-stage liver diseases, such as hepatocellular carcinoma. We also provide evidence and models by which other viruses such as HIV and Zika disrupt their host metabolic machinery. The emergence of the immunometabolism field provides novel opportunities to take advantage of intermediary metabolites and key metabolic pathways for diagnostic and therapeutic purposes.

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“…In this setting, brain energetic failure could potentially be the cause of ZIKV congenital malformations, as similar phenotypes are exhibited in Glut‐1 deficiency syndrome (Jensen et al. ; Blonz, ; Solomon et al. ; Tang et al.…”

Section: Cellular Changes Damage and Death In The Cns During Zikv Inmentioning

confidence: 89%

“…Energetic deficit due to glucose impairment has a direct negative impact on human brain development and is therefore of potential consideration in ZIKV infection, particularly during the first trimester of pregnancy. As Blonz () hypothesised, a high‐fat metabolism might prevent congenital abnormalities due to glucose impairment. Here we highlighted a potential link between cellular glucose impairment and different cellular alterations exhibited during ZIKV infection, emphasising that a ketone metabolism, as an efficient brain alternative fuel with positive effects in human physiology (Klepper et al.…”

Section: Potential Nutritional Intervention To Prevent Zikv Replicatimentioning

confidence: 99%

The potential contribution of impaired brain glucose metabolism to congenital Zika syndrome

et al. 2019

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The Zika virus (ZIKV) became a major worldwide public concern in 2015 due to the congenital syndrome which presents the highest risk during the first trimester of pregnancy and includes microcephaly and eye malformations. Several cellular, genetic and molecular studies have shown alterations in metabolic pathways, endoplasmic reticulum (ER) stress, immunity and dysregulation of RNA and energy metabolism both in vivo and in vitro. Here we summarise the main metabolic complications, with a particular focus on the possibility that brain energy metabolism is altered following ZIKV infection, contributing to developmental abnormalities. Brain energetic failure has been implicated in neurological conditions such as autism disorder and epilepsy, as well as in metabolic diseases with severe neurodevelopmental complications such as Glut‐1 deficiency syndrome. Therefore, these energetic alterations are of wide‐ranging interest as they might be directly implicated in congenital ZIKV syndrome. Data showing increased glycolysis during ZIKV infection, presumably required for viral replication, might support the idea that the virus can cause energetic stress in the developing brain cells. Consequences may include neuroinflammation, cell cycle dysregulation and cell death. Ketone bodies are non‐glycolytic brain fuels that are produced during neonatal life, starvation or fasting, ingestion of high‐fat low‐carbohydrate diets, and following supplementation with ketone esters. We propose that dietary ketones might alter the course of the disease and could even provide some degree of prevention of ZIKV‐associated abnormalities and potentially related neurological conditions characterised by brain glucose impairment.

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Zika virus and GLUT1

Cited by 10 publications

References 7 publications

Exploiting immune cell metabolic machinery for functional HIV cure and the prevention of inflammaging

Exploiting immune cell metabolic machinery for functional HIV cure and the prevention of inflammaging

Metabolic reprogramming during hepatitis B disease progression offers novel diagnostic and therapeutic opportunities

The potential contribution of impaired brain glucose metabolism to congenital Zika syndrome

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